Quantifying walking speeds in relation to ankle biomechanics on a real-time interactive gait platform: a musculoskeletal modeling approach in healthy adults.

Background: Given the inherent variability in walking speeds encountered in day-to-day activities, understanding the corresponding alterations in ankle biomechanics would provide valuable clinical insights. Therefore, the objective of this study was to examine the influence of different walking speeds on biomechanical parameters, utilizing gait analysis and musculoskeletal modelling. Methods: Twenty healthy volunteers without any lower limb medical history were included in this study. Treadmill-assisted gait-analysis with walking speeds of 0.8 m/s and 1.1 m/s was performed using the Gait Real-time Analysis Interactive Lab (GRAIL®). Collected kinematic data and ground reaction forces were processed via the AnyBody® modeling system to determine ankle kinetics and muscle forces of the lower leg. Data were statistically analyzed using statistical parametric mapping to reveal both spatiotemporal and magnitude significant differences. Results: Significant differences were found for both magnitude and spatiotemporal curves between 0.8 m/s and 1.1 m/s for the ankle flexion (p < 0.001), subtalar force (p < 0.001), ankle joint reaction force and muscles forces of the M. gastrocnemius, M. soleus and M. peroneus longus (α = 0.05). No significant spatiotemporal differences were found between 0.8 m/s and 1.1 m/s for the M. tibialis anterior and posterior. Discussion: A significant impact on ankle joint kinematics and kinetics was observed when comparing walking speeds of 0.8 m/s and 1.1 m/s. The findings of this study underscore the influence of walking speed on the biomechanics of the ankle. Such insights may provide a biomechanical rationale for several therapeutic and preventative strategies for ankle conditions.

Validation of a personalized ligament-constraining discrete element framework for computing ankle joint contact mechanics.

BACKGROUND AND OBJECTIVE: Computer simulations of joint contact mechanics have great merit to improve our current understanding of articular ankle pathology. Owed to its computational simplicity, discrete element analysis (DEA) is an encouraging alternative to finite element analysis (FEA). However, previous DEA models lack subject-specific anatomy and may oversimplify the biomechanics of the ankle. The objective of this study was to develop and validate a personalized DEA framework that permits movement of the fibula and incorporates personalized cartilage thickness as well as ligamentous constraints. METHODS: A linear and non-linear DEA framework, representing cartilage as compressive springs, was established, verified, and validated. Three-dimensional (3D) bony ankle models were constructed from cadaveric lower limb CT scans imaged during application of weight (85 kg) and/or torque (10 Nm). These 3D models were used to generate cartilage thickness and ligament insertion sites based on a previously validated statistical shape model. Ligaments were modelled as non-linear tension-only springs. Validation of contact stress prediction was performed using a simple, axially constrained tibiotalar DEA model against an equivalent FEA model. Validation of ligamentous constraints compared the final position of the ankle mortise to that of the cadaver after application of torque and sequential ligament sectioning. Finally, a combined ligamentous-constraining DEA model was validated for predicted contact stress against an equivalent ligament-constraining FEA model. RESULTS: The linear and non-linear DEA model reproduced a mean articular contact stress within 0.36 MPa and 0.39 MPa of the FEA calculated stress, respectively. With respect to the ligamentous validation, the DEA ligament-balancing algorithm could reproduce the position of the distal fibula within the ankle mortise to within 0.97 mm of the experimental observed distal fibula. When combining the ligament-constraining and contact stress algorithm, DEA was able to reproduce a mean articular contact stress to within 0.50 MPa of the FEA calculated contact stress. CONCLUSION: The DEA framework presented herein offers a computationally efficient alternative to FEA for the prediction of contact stress in the ankle joint, manifesting its potential to enhance the mechanical understanding of articular ankle pathologies on both a patient-specific and population-wide level. The novelty of this model lies in its personalized nature, inclusion of the distal tibiofibular joint and the use of non-linear ligament balancing to maintain the physiological ankle joint articulation.

Personalised statistical modelling of soft tissue structures in the ankle.

BACKGROUND AND OBJECTIVE: Revealing the complexity behind subject-specific ankle joint mechanics requires simultaneous analysis of three-dimensional bony and soft-tissue structures. 3D musculoskeletal models have become pivotal in orthopedic treatment planning and biomechanical research. Since manual segmentation of these models is time-consuming and subject to manual errors, (semi-) automatic methods could improve the accuracy and enlarge the sample size of personalised 'in silico' biomechanical experiments and computer-assisted treatment planning. Therefore, our aim was to automatically predict ligament paths, cartilage topography and thickness in the ankle joint based on statistical shape modelling. METHODS: A personalised cartilage and ligamentous prediction algorithm was established using geometric morphometrics, based on an 'in-house' generated lower limb skeletal model (N = 542), tibiotalar cartilage (N = 60) and ankle ligament segmentations (N = 10). For cartilage, a population-averaged thickness map was determined by use of partial least-squares regression. Ligaments were wrapped around bony contours based on iterative shortest path calculation. Accuracy of ligament path and cartilage thickness prediction was quantified using leave-one-out experiments. The novel personalised thickness prediction was compared with a constant cartilage thickness of 1.50 mm by use of a paired sample T-test. RESULTS: Mean distance error of cartilage and ligament prediction was 0.12 mm (SD 0.04 mm) and 0.54 mm (SD 0.05 mm), respectively. No significant differences were found between the personalised thickness cartilage and segmented cartilage of the tibia (p = 0.73, CI [-1.60 .10-17, 1.13 .10-17]) and talus (p = 0.95, CI[ -1.35 .10-17, 1.28 .10-17]). For the constant thickness cartilage, a statistically significant difference was found in 89% and 92% of the tibial (p < 0.001, CI [0.51, 0.58]) and talar (p < 0.001, CI [0.33, 0.40]) cartilage area. CONCLUSIONS: In this study, we described a personalised prediction algorithm of cartilage and ligaments in the ankle joint. We were able to predict cartilage and main ankle ligaments with submillimeter accuracy. The proposed method has a high potential for generating large (virtual) sample sizes in biomechanical research and mitigates technological advances in computer-assisted orthopaedic surgery.

Association between knee inflammation and knee pain in patients with knee osteoarthritis: a systematic review.

OBJECTIVE: To systematically review the literature on the relationship between markers of inflammation and pain in patients with knee osteoarthritis (OA). METHODS: We searched MEDLINE, Web of Science and EMBASE databases from inception until June 2021. Eligible articles had to report on the association between inflammation (as measured by effusion, synovitis, baker's cysts, cytokines and C-reactive protein) and pain in patients with radiographic knee OA. Two reviewers independently performed a screening on title and abstracts, data extraction and risk of bias assessment using the Newcastle-Ottawa Scale (NOS). A best evidence synthesis was conducted for each inflammatory sign included in this review. RESULTS: 37 studies were included. Articles reported on the following measures: effusion or synovitis assessed via ultrasound (n = 9) or magnetic resonance imaging (MRI) (n = 17); baker's cyst (n = 3); cytokine concentrations (n = 11); and C-reactive protein levels (n = 4). The strength of the association between inflammation and pain does not exceed the moderate level (i.e., correlation coefficient values ranging from 0.19 to 0.61). Moderate levels of evidence were found for the association between synovitis (measured with ultrasound or contrast enhanced MRI) and pain. The levels of evidence between effusion (assessed via ultrasound), effusion/synovitis (assessed via non-contrast enhanced MRI), Baker's cyst, cytokines, C-reactive protein and pain were conflicting. CONCLUSIONS: Different inflammatory markers are associated with pain but the correlation ranges from weak to moderate, and the quality of evidence from conflicting to moderate. Further research is needed to strengthen the level of evidence and to establish mechanisms.